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Hypothermia is not therapeutic in a neonatal piglet model of inflammation-sensitized hypoxia-ischemia

Martinello, K. A. (author)
Meehan, C. (author)
Avdic-Belltheus, A. (author)
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Lingam, I. (author)
Mutshiya, T. (author)
Yang, Q. (author)
Akin, M. A. (author)
Price, D. (author)
Sokolska, M. (author)
Bainbridge, A. (author)
Hristova, M. (author)
Tachtsidis, I. (author)
Tann, C. J. (author)
Peebles, D. (author)
Hagberg, Henrik, 1955 (author)
Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper, Avdelningen för obstetrik och gynekologi,Institute of Clinical Sciences, Department of Obstetrics and Gynecology
Wolfs, Tgam (author)
Klein, N. (author)
Kramer, B. W. (author)
Fleiss, B. (author)
Gressens, P. (author)
Golay, X. (author)
Robertson, N. J. (author)
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 (creator_code:org_t)
2021-05-28
2022
English.
In: Pediatric Research. - : Springer Science and Business Media LLC. - 0031-3998 .- 1530-0447. ; 91:6, s. 1416-1427
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  • Journal article (peer-reviewed)
Abstract Subject headings
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  • BACKGROUND: Perinatal inflammation combined with hypoxia-ischemia (HO exacerbates injury in the developing brain. Therapeutic hypothermia (HT) is standard care for neonatal encephalopathy; however, its benefit in inflammation-sensitized HI (IS-HI) is unknown. METHODS: Twelve newborn piglets received a 2 mu g/kg bolus and 1 mu g/kg/h infusion over 52 h of Escherichia coli lipopolysaccharide (LPS). HI was induced 4 h after LPS bolus. After HI, piglets were randomized to HT (33.5 degrees C 1-25 h after HI, n = 6) or normothermia (NT, n = 6). Amplitude-integrated electroencephalogram (aEEG) was recorded and magnetic resonance spectroscopy (MRS) was acquired at 24 and 48 h. At 48 h, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL)-positive brain cell death, microglial activation/proliferation, astrogliosis, and cleaved caspase-3 (CC3) were quantified. Hematology and plasma cytokines were serially measured. RESULTS: Two HT piglets died. aEEG recovery, thalamic and white matter MRS lactate/N-acetylaspartate, and TUNEL-positive cell death were similar between groups. HT increased microglial activation in the caudate, but had no other effect on glial activation/ proliferation. HT reduced CC3 overall. HT suppressed platelet count and attenuated leukocytosis. Cytokine profile was unchanged by HT. CONCLUSIONS: We did not observe protection with HT in this piglet IS-HI model based on aEEG, MRS, and immunohistochemistry. immunosuppressive effects of HT and countering neuroinflammation by LPS may contribute to the observed lack of HT efficacy. Other immunomodulatory strategies may be more effective in IS-HI.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Pediatrik (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Pediatrics (hsv//eng)

Keyword

cerebral energy failure
brain-injury
clinical-trial
encephalopathy
outcomes
infection
infants
lipopolysaccharide
mechanisms
cytokine
Pediatrics

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ref (subject category)
art (subject category)

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